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A double-edged sword: The HBV-induced non-coding RNAs alterations in hepatocellular carcinoma


1 Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, M5S1A1, Canada
2 State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China

* Corresponding Author: Hongyan Diao,

BIOCELL 2023, 47(1), 27-32.


Non-coding RNAs are speculated to exert important regulatory functions at the level of gene expression, oncogenesis, and many other pathologies. Hepatitis B virus (HBV) infection is a leading cause of hepatocellular carcinoma (HCC), and some studies have shown that the expression of non-coding RNAs has an assignable effect on the development of HBV-induced HCC. In this context, the functions and molecular mechanisms of the HBVinduced non-coding RNA expression in the development of hepatoma have attracted increasing attention. This review covers the progress in the exploration of the relationship between HBV-induced hepatoma and non-coding RNA expression, cataloging the recent reports about the roles of non-coding RNAs in HBV-induced hepatoma into five classes, including (1) modulation of metabolism in hepatic cancer, (2) aggravation of inflammation and hepatic fibrosis, (3) alteration of the tumor immune microenvironment, (4) non-coding RNA N6-methyladenosine modification, and a seemingly opposite process, (5) the suppression of the progression of HBV-related HCC. All evidence supports non-coding RNAs as promising novel targets for the early diagnosis and treatments for HCC.


Cite This Article

LIU, T., DIAO, H. (2023). A double-edged sword: The HBV-induced non-coding RNAs alterations in hepatocellular carcinoma. BIOCELL, 47(1), 27–32.

This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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